Cocaine Information,
Use, Testing and Treatment

Cocaine
(benzoylmethyl ecgonine) is a crystalline tropane alkaloid that is
obtained from the leaves of the coca plant. The name comes from
"coca" in addition to the alkaloid suffix -ine, forming cocaine.
It is both a stimulant of the central nervous system and an appetite
suppressant. Specifically, it is a dopamine reuptake inhibitor, a norepinephrine
reuptake inhibitor and a serotonin reuptake inhibitor which mediates
functionality of such as an exogenous
DAT ligand.
Because of the way it affects the mesolimbic reward pathway, cocaine is
addictive.

Its possession,
cultivation, and distribution are illegal for non-medicinal and non-government
sanctioned purposes in virtually all parts of the world. Although its free
commercialization is illegal and has been severely penalized in virtually all
countries, its use worldwide remains widespread in many social, cultural, and
personal settings.

History of
Cocaine

Coca leaf

For over a
thousand years South American indigenous peoples have chewed the coca leaf (Erythroxylon
coca), a plant that contains vital nutrients as well as numerous alkaloids,
including cocaine. The leaf was, and is, chewed almost universally by some
indigenous communities—ancient Peruvian mummies have been found with the remains
of coca leaves, and pottery from the time period depicts humans, cheeks bulged
with the presence of something on which they are chewing. There is
also evidence that these cultures used a mixture of coca leaves and saliva as an
anesthetic for the performance of trepanation.

The coca plant,
Erythroxylon coca.

When the
Spaniards conquered South America, they at first ignored aboriginal claims that
the leaf gave them strength and energy, and declared the practice of chewing it
the work of the Devil.But after discovering that these claims were
true, they legalized and taxed the leaf, taking 10% off the value of each crop. In 1569, Nicolás Monardes described the practice of the natives of
chewing a mixture of tobacco and coca leaves to induce "great contentment":

In 1609, Padre
Blas Valera wrote: “Coca protects the
body from many ailments, and our doctors use it in powdered form to reduce the
swelling of wounds, to strengthen broken bones, to expel cold from the body or
prevent it from entering, and to cure rotten wounds or sores that are full of
maggots. And if it does so much for outward ailments, will not its singular
virtue have even greater effect in the entrails of those who eat it?”

Isolation

Although the
stimulant and hunger-suppressant properties of coca had been known for many
centuries, the isolation of the cocaine alkaloid was not achieved until 1855 .
Many scientists had attempted to isolate cocaine, but none had been successful
for two reasons: the knowledge of chemistry required was insufficient at the
time, and the cocaine was worsened because coca does not grow in Europe and
ruins easily during travel.

The cocaine
alkaloid was first isolated by the German chemist Friedrich Gaedcke in 1855.
Gaedcke named the alkaloid "erythroxyline", and published a description in the
journal Archiv der Pharmazie.

In 1856,
Friedrich Wöhler asked Dr. Carl Scherzer, a scientist aboard the Novara
(an Austrian frigate sent by Emperor Franz Joseph to circle the globe), to bring
him a large amount of coca leaves from South America. In 1859, the ship finished
its travels and Wöhler received a trunk full of coca. Wöhler passed on the
leaves to Albert Niemann, a Ph.D. student at the University of Göttingen in
Germany, who then developed an improved purification process.

Niemann
described every step he took to isolate cocaine in his dissertation titled
Über eine neue organische Base in den Cocablättern (On a New Organic Base
in the Coca Leaves), which was published in 1860—it earned him his Ph.D. and
is now in the British Library. He wrote of the alkaloid's “colourless
transparent prisms” and said that, “Its solutions have an alkaline reaction, a
bitter taste, promote the flow of saliva and leave a peculiar numbness, followed
by a sense of cold when applied to the tongue.” Niemann named the alkaloid
“cocaine”—as with other alkaloids its name carried the “-ine” suffix (from Latin
-ina).

The first
synthesis and elucidation of the structure of the cocaine molecule was by
Richard Willstätter in 1898. The synthesis started from tropinone, a
related natural product and took five steps.

Medicalization

With the
discovery of this new alkaloid, Western medicine was quick to exploit the
possible uses of this plant.

In 1879, Vassili
von Anrep, of the University of Würzburg, devised an experiment to demonstrate
the analgesic properties of the newly-discovered alkaloid. He prepared two
separate jars, one containing a cocaine-salt solution, with the other containing
merely salt water. He then submerged a frog's legs into the two jars, one leg in
the treatment and one in the control solution, and proceeded to stimulate the
legs in several different ways. The leg that had been immersed in the cocaine
solution reacted very differently than the leg that had been immersed in salt
water.

Carl Koller (a
close associate of Sigmund Freud, who would write about cocaine later)
experimented with cocaine for ophthalmic usage. In an infamous experiment in
1884, he experimented upon himself by applying a cocaine solution to his own eye
and then pricking it with pins. His findings were presented to the Heidelberg
Ophthalmological Society. Also in 1884, Jellinek demonstrated the effects of
cocaine as a respiratory system anesthetic. In 1885, William Halsted
demonstrated nerve-block anesthesia, and James Corning demonstrated
peridural anesthesia. 1898 saw Heinrich Quincke use cocaine for
spinal anaesthesia.

Popularization

In 1859, an
Italian doctor, Paolo Mantegazza, returned from Peru, where he had witnessed
first-hand the use of coca by the natives. He proceeded to experiment on himself
and upon his return to Milan he wrote a paper in which he described the effects.
In this paper he declared coca and cocaine (at the time they were assumed to be
the same) as being useful medicinally, in the treatment of “a furred tongue in
the morning, flatulence, [and] whitening of the teeth.”

A chemist named
Angelo Mariani who read Mantegazza’s paper became immediately intrigued with
coca and its economic potential. In 1863, Mariani started marketing a wine
called Vin Mariani, which had been treated with coca leaves, to become cocawine.
The ethanol in wine acted as a solvent and extracted the cocaine from the coca
leaves, altering the drink’s effect. It contained 6 mg cocaine per ounce of
wine, but Vin Mariani which was to be exported contained 7.2 mg per ounce, to
compete with the higher cocaine content of similar drinks in the United States.
A “pinch of coca leaves” was included in John Styth Pemberton's original 1886
recipe for Coca-Cola, though the company began using decocainized leaves in 1906
when the Pure Food and Drug Act was passed. The actual amount of cocaine that
Coca-Cola contained during the first twenty years of its production is
practically impossible to determine.

In 1879 cocaine
began to be used to treat morphine addiction. Cocaine was introduced into
clinical use as a local anaesthetic in Germany in 1884, about the same time as
Sigmund Freud published his work Über Coca, in which he wrote that
cocaine causes: “...exhilaration and
lasting euphoria, which in no way differs from the normal euphoria of the
healthy person...You perceive an increase of self-control and possess more
vitality and capacity for work....In other words, you are simply normal, and it
is soon hard to believe you are under the influence of any drug....Long
intensive physical work is performed without any fatigue...This result is
enjoyed without any of the unpleasant after-effects that follow exhilaration
brought about by alcohol....Absolutely no craving for the further use of cocaine
appears after the first, or even after repeated taking of the drug...”

Cocaine, the
fast-acting anesthetic.

In 1885 the U.S.
manufacturer Parke-Davis sold cocaine in various forms, including cigarettes,
powder, and even a cocaine mixture that could be injected directly into the
user’s veins with the included needle. The company promised that its cocaine
products would “supply the place of food, make the coward brave, the silent
eloquent and ... render the sufferer insensitive to pain.”

By the late
Victorian era cocaine use had appeared as a vice in literature, for example it
was injected by Arthur Conan Doyle’s fictional Sherlock Holmes.

In early
20th-century Memphis, Tennessee, cocaine was sold in neighborhood drugstores on
Beale Street, costing five or ten cents for a small boxful. Stevedores along the
Mississippi River used the drug as a stimulant, and white employers encouraged
its use by black laborers.

In 1909, Ernest
Shackleton took “Forced March” brand cocaine tablets to Antarctica, as did
Captain Scott a year later on his ill-fated journey to the South Pole.

Prohibition

By the turn of
the twentieth century, the addictive properties of cocaine had become clear, and
the problem of cocaine abuse began to capture public attention in the United
States. The dangers of cocaine abuse became part of a moral panic that was tied
to the dominant racial and social anxieties of the day. In 1903, the American
Journal of Pharmacy stressed that most cocaine abusers were “bohemians,
gamblers, high- and low-class prostitutes, night porters, bell boys, burglars,
racketeers, pimps, and casual laborers.” In 1914, Dr. Christopher Koch of
Pennsylvania’s State Pharmacy Board made the racial innuendo explicit,
testifying that, “Most of the attacks upon the white women of the South are the
direct result of a cocaine-crazed Negro brain.” Mass media manufactured an
epidemic of cocaine use among African Americans in the Southern United States to
play upon racial prejudices of the era, though there is little evidence that
such an epidemic actually took place. In the same year, the Harrison Narcotics
Tax Act outlawed the sale and distribution of cocaine in the United States. This
law incorrectly referred to cocaine as a narcotic, and the misclassification
passed into popular culture. As stated above, cocaine is a stimulant, not a
narcotic. Although technically illegal for purposes of distribution and use, the
distribution, sale and use of cocaine was still legal for registered companies
and individuals. Because of the misclassification of cocaine as a narcotic, the
debate is still open on whether the government actually enforced these laws
strictly. Cocaine was not considered a controlled substance until 1970, when the
United States listed it as such in the Controlled Substances Act. Until that
point, the use of cocaine was open and rarely prosecuted in the US due to the
moral and physical debates commonly discussed.

Modern usage

In many
countries, cocaine is a popular recreational drug. In the United States, the
development of "crack" cocaine introduced the substance to a generally poorer
inner-city market. Use of the powder form has stayed relatively constant,
experiencing a new height of use during the late 1990s and early 2000s in the
U.S., and has become much more popular in the last few years in the UK.

Cocaine use is
prevalent across all socioeconomic strata, including age, demographics,
economic, social, political, religious, and livelihood.

The estimated
U.S. cocaine market exceeded $70 billion in street value for the year 2005,
exceeding revenues by corporations such as Starbucks. There is a
tremendous demand for cocaine in the U.S. market, particularly among those who
are making incomes affording luxury spending, such as single adults and
professionals with discretionary income. Cocaine’s status as a club drug shows
its immense popularity among the “party crowd”.

In 1995 the
World Health Organization (WHO) and the United Nations Interregional Crime and
Justice Research Institute (UNICRI) announced in a press release the publication
of the results of the largest global study on cocaine use ever undertaken.
However, a decision in the World Health Assembly banned the publication of the
study. In the sixth meeting of the B committee the US representative threatened
that "If WHO activities relating to drugs failed to reinforce proven drug
control approaches, funds for the relevant programs should be curtailed". This
led to the decision to discontinue publication. A part of the study has been
recuperated. Available are profiles of cocaine use in 20 countries.

A problem with
illegal cocaine use, especially in the higher volumes used to combat fatigue
(rather than increase euphoria) by long-term users is the risk of ill effects or
damage caused by the compounds used in adulteration. Cutting or "stamping on"
the drug is commonplace, using compounds which simulate ingestion effects, such
as Novocain (procaine) producing temporary anaesthaesia as many users believe a
strong numbing effect is the result of strong and/or pure cocaine, ephedrine or
similar stimulants that are to produce an increased heart rate. The normal
adulterants for profit are inactive sugars, usually mannitol, creatine or
glucose, so introducing active adulterants gives the illusion of purity and to
'stretch' or make it so a dealer can sell more product than without the
adulterants. The adulterant of sugars therefore allows the dealer to sell the
product for a higher price because of the illusion of purity and allows to sell
more of the product at that higher price, enabling dealers to make a lot of
revenue with little cost of the adulterants. Cocaine trading carries large
penalties in most jurisdictions, so user deception about purity and consequent
high profits for dealers are the norm.

Cocaine Pharmacology

Appearance

A pile of
cocaine hydrochloride

A piece of
compressed cocaine powder

Cocaine in its
purest form is a white, pearly product. Cocaine appearing in powder form is a
salt, typically cocaine hydrochloride (CAS 53-21-4). Street market cocaine is
frequently adulterated or “cut” with various powdery fillers to increase its
weight; the substances most commonly used in this process are baking soda;
sugars, such as lactose, dextrose, inositol, and mannitol; and local
anesthetics, such as lidocaine or benzocaine, which mimic or add to cocaine's
numbing effect on mucous membranes. Cocaine may also be "cut" with other
stimulants such as methamphetamine. Adulterated cocaine is often a white,
off-white or pinkish powder.

The color of
“crack” cocaine depends upon several factors including the origin of the cocaine
used, the method of preparation – with ammonia or baking soda – and the presence
of impurities, but will generally range from white to a yellowish cream to a
light brown. Its texture will also depend on the adulterants, origin and
processing of the powdered cocaine, and the method of converting the base. It
ranges from a crumbly texture, sometimes extremely oily, to a hard, almost
crystalline nature.

Forms of cocaine

Cocaine
sulfate

Cocaine sulfate
is produced by macerating coca leaves along with water that has been acidulated
with sulfuric acid, or an aromatic-based solvent, like kerosene or benzene. This
is often accomplished by placing the ingredients into a vat and stomping on
them, in a manner similar to the traditional method for crushing grapes. A more
popular method in modern times is to form a makeshift "vat" by spreading a heavy
nylon tarp on the floor of an enclosed area and shred the leaves with a
gas-powered weed trimmer. This method is fast, and not only shreds the leaves,
but results in bruising and fragmenting of the remaining pieces, aiding the
extraction process. After the maceration is completed, the water is evaporated
to yield a pasty mass of impure cocaine sulfate. The sulfate salt itself is an
intermediate step to producing cocaine hydrochloride.

Freebase

As the name
implies, “freebase” is the base form of cocaine, as opposed to the salt form of
cocaine hydrochloride. Whereas cocaine hydrochloride is extremely soluble in
water, cocaine base is insoluble in water and is therefore not suitable for
drinking, snorting or injecting. Whereas cocaine hydrochloride is not
well-suited for smoking because the temperature at which it vaporizes is very
high and close to the temperature at which it burns; cocaine base vaporizes at a
much lower temperature, which makes it suitable for inhalation.

Smoking freebase
cocaine has the additional effect of releasing methylecgonidine into the user's
system due to the pyrolysis of the substance (a side effect which insufflating
or injecting powder cocaine does not create). Some research suggests that
smoking freebase cocaine can be even more cardiotoxic than other routes of
administration because of methylecgonidine's effects on lung tissue and liver tissue.

Smoking freebase
is a popular route of ingestion because the cocaine is absorbed immediately into
blood via the lungs, reaching the brain in about five seconds. The rush is much
more intense than snorting the same amount of cocaine nasally, but the effects
do not last as long. The peak of the freebase rush is over almost as soon as the
user exhales the vapor, but the high typically lasts 5–10 minutes afterward.
What makes freebasing particularly dangerous is that users typically do not wait
that long for their next hit and will continue to smoke freebase until none is
left. These effects are similar to those that can be achieved by injecting or
“slamming” cocaine hydrochloride, but without the risks associated with
intravenous drug use (though there are other serious risks associated with
smoking freebase).

Freebase cocaine
is produced by first dissolving cocaine hydrochloride in water. Once dissolved
in water, cocaine hydrochloride (Coc-HCl) dissociates into the protonated
cocaine ion (Coc-H+) and the chloride ion (Cl−). Any
solids that remain suspended in the solution are impurities from the cut and are
removed by filtration. A base, typically ammonia (NH3), is added to
the solution. The following net acid-base reaction takes place:

Coc-H+ + NH3 →
Coc + NH4+

As freebase
cocaine (Coc) is insoluble in water, it precipitates and the solution becomes
cloudy. To recover the freebase in the "traditional" manner, diethyl ether is
added to the solution. Since freebase is highly soluble in ether, a vigorous
shaking of the mixture results in the freebase being dissolved in the ether. As
ether is practically insoluble in water, it can be siphoned off. The ether is
then left to evaporate, leaving behind the nearly pure freebase.

Handling diethyl
ether is dangerous because ether is extremely flammable; its vapors are heavier
than air and can "creep" from an open bottle, and in the presence of oxygen it
can form peroxides, which can spontaneously combust. Comedian Richard Pryor
performed a skit poking fun at himself for a 1980 incident in which he caused an
explosion and ignited himself attempting to smoke "freebase", presumably while
still wet with ether (though his ex-wife Jennifer Lee Pryor said that he poured
high-proof rum
over his body and torched himself in a drug psychosis).

Crack cocaine

Smoking crack
cocaine.

In its creation
process, due to the dangers of using ether to produce pure freebase cocaine,
cocaine producers began to omit the step of removing the freebase cocaine
precipitate from the ammonia mixture. Typically, filtration processes are also
omitted. The end result of this process is that the cut, in addition to the
ammonium salt (NH4Cl),
remains in the freebase cocaine after the mixture is evaporated. The “rock” that
is thus formed also contains a small amount of water. Sodium bicarbonate (baking
soda) is also preferred in preparing the freebase, for when commonly
"cooked" the ratio is 50/50 to 40/60% cocaine/bicarbonate. This acts as a filler
which extends the overall profitability of illicit sales. Crack cocaine may be
reprocessed in small quantities with water (users refer to the resultant product
as "cookback"). This removes the residual bicarbonate, and any adulterants or
cuts that have been used in the previous handling of the cocaine and leaves a
relatively pure, anhydrous cocaine base.

When the rock is
heated, this water boils, making a crackling sound (hence the onomatopoeic
“crack”). Baking soda is now most often used as a base rather than ammonia for
reasons of lowered stench and toxicity; however, any weak base can be used to
make crack cocaine. Strong bases, such as sodium hydroxide, tend to hydrolyze
some of the cocaine into non-psychoactive ecgonine.

Coca leaf
infusions

Coca herbal
infusion (also referred to as Coca tea) is used in coca-leaf producing countries
much as any herbal medicinal infusion would elsewhere in the world. The free and
legal commercialization of dried coca leaves under the form of filtration bags
to be used as "coca tea" has been actively promoted by the governments of Peru
and Bolivia for many years as a drink having medicinal powers. Visitors to the
city of Cuzco in Peru, and La Paz in Bolivia are greeted with the offering of
coca leaf infusions (prepared in tea pots with whole coca leaves) purportedly to
help the newly-arrived traveler overcome the malaise of high altitude sickness.
The effects of drinking coca tea are a mild stimulation and mood lift. It does
not produce any significant numbing of the mouth nor does it give a rush like
snorting cocaine. In order to prevent the demonization of this product, its
promoters publicize the unproven concept that much of the effect of the
ingestion of coca leaf infusion would come from the secondary alkaloids, as
being not only quantitatively different from pure cocaine but also qualitatively
different.

It has been
promoted as an adjuvant for the treatment of cocaine dependence. In one
controversial study, coca leaf infusion was used -in addition to counseling- to
treat 23 addicted coca-paste smokers in Lima, Peru. Relapses fell from an
average of four times per month before treatment with coca tea to one during the
treatment. The duration of abstinence increased from an average of 32 days prior
to treatment to 217 days during treatment. These results suggest that the
administration of coca leaf infusion plus counseling would be an effective
method for preventing relapse during treatment for cocaine addiction.
Importantly, these results also suggest strongly that the primary
pharmacologically active metabolite in coca leaf infusions is actually cocaine
and not the secondary alkaloids.

The cocaine
metabolite benzoylecgonine can be detected in the urine of people a few hours
after drinking one cup of coca leaf infusion.

Many users rub
the powder along the gum line, or onto a cigarette filter which is then smoked
(called a "hoolie"), which numbs the gums and teeth - hence the colloquial names
of "numbies", "gummers" or "cocoa puffs" for this type of administration. This
is mostly done with the small amounts of cocaine remaining on a surface after
insufflation. Another oral method is to wrap up some cocaine in rolling paper
and swallow it. This is sometimes called a "snow bomb."

Coca leaf

Coca leaves are
typically mixed with an alkaline substance (such as lime) and chewed into a wad
that is retained in the mouth between gum and cheek (much in the same as chewing
tobacco is chewed) and sucked of its juices. The juices are absorbed slowly by
the mucous membrane of the inner cheek and by the gastrointestinal tract when
swallowed. Alternatively, coca leaves can be infused in liquid and consumed like
tea. Ingesting coca leaves generally is an inefficient means of administering
cocaine. Advocates of the consumption of the coca leaf state that coca leaf
consumption should not be criminalized as it is not actual cocaine, and
consequently it is not properly the illicit drug. Because cocaine is hydrolyzed
and rendered inactive in the acidic stomach, it is not readily absorbed when
ingested alone. Only when mixed with a highly alkaline substance (such as lime)
can it be absorbed into the bloodstream through the stomach. The efficiency of
absorption of orally administered cocaine is limited by two additional factors.
First, the drug is partly catabolized by the liver. Second, capillaries in the
mouth and esophagus constrict after contact with the drug, reducing the surface
area over which the drug can be absorbed. Nevertheless, cocaine metabolites can
be detected in the urine of subjects that have sipped even one cup of coca leaf
infusion. Therefore, this is an actual additional form of administration of
cocaine, albeit an inefficient one.

Orally
administered cocaine takes approximately 30 minutes to enter the bloodstream.
Typically, only a third of an oral dose is absorbed, although absorption has
been shown to reach 60% in controlled settings. Given the slow rate of
absorption, maximum physiological and psychotropic effects are attained
approximately 60 minutes after cocaine is administered by ingestion. While the
onset of these effects is slow, the effects are sustained for approximately 60
minutes after their peak is attained.

Contrary to
popular belief, both ingestion and insufflation result in approximately the same
proportion of the drug being absorbed: 30 to 60%. Compared to ingestion, the
faster absorption of insufflated cocaine results in quicker attainment of
maximum drug effects. Snorting cocaine produces maximum physiological effects
within 40 minutes and maximum psychotropic effects within 20 minutes, however, a
more realistic activation period is closer to 5 to
10 minutes, which is similar to ingestion of cocaine.
Physiological and psychotropic effects from nasally insufflated cocaine are
sustained for approximately 40 - 60
minutes after the peak effects are attained.

Mate de coca
or coca-leaf infusion is also a traditional method of consumption and is often
recommended in coca producing countries, like Peru and Bolivia, to ameliorate
some symptoms of altitude sickness. This method of consumption has been
practiced for many centuries by the native tribes of South America. One specific
purpose of ancient coca leaf consumption was to increase energy and reduce
fatigue in messengers who made multi-day quests to other settlements.

In 1986 an
article in the Journal of the American Medical Association revealed that
U.S. health food stores were selling dried coca leaves to be prepared as an
infusion as “Health Inca Tea.” While the packaging claimed it had
been “decocainized,” no such process had actually taken place. The article
stated that drinking two cups of the tea per day gave a mild stimulation,
increased heart rate, and
mood
elevation, and the tea was essentially harmless. Despite this, the DEA seized
several shipments in Hawaii, Chicago, Illinois, Georgia, and several locations
on the East Coast of the United States, and the product was removed from the
shelves.

Insufflation

A man snorting
cocaine with a rolled up dollar bill, 2007.

Insufflation
(known colloquially as "snorting," "sniffing," or "blowing") is the most common
method of ingestion of recreational powdered cocaine in the Western world. The
drug coats and is absorbed through the mucous membranes lining the sinuses. When
insufflating cocaine, absorption through the nasal membranes is approximately
30–60%, with higher doses leading to increased absorption efficiency. Any
material not directly absorbed through the mucous membranes is collected in
mucus and swallowed (this "drip" is considered pleasant by some and unpleasant
by others). In a study of cocaine users, the average time taken to
reach peak subjective effects was 14.6 minutes. Any damage to the inside of the
nose is because cocaine highly constricts blood vessels – and therefore blood
and oxygen/nutrient flow – to that area.

Prior to
insufflation, cocaine powder must be divided into very fine particles. Cocaine
of high purity breaks into fine dust very easily, except when it is moist (not
well stored) and forms "chunks," which reduces the efficiency of nasal
absorption.

Rolled up
banknotes, hollowed-out pens, cut straws, pointed ends of keys, specialized
spoons, long fingernails, and (clean) tampon applicators are often used to
insufflate cocaine. Such devices are often called "tooters" by users. The
cocaine typically is poured onto a flat, hard surface (such as a mirror, CD case
or book) and divided into "bumps", "lines" or "rails", and then insufflated. As tolerance builds rapidly in the short-term (hours), many lines are
often snorted to produce greater effects.

A study by
Bonkovsky and Mehta reported that, just like shared needles, the
sharing of straws used to "snort" cocaine can spread blood diseases such as
Hepatitis C.

In the United
States, as far back as 1992 many of the people sentenced by federal authorities
for charges related to powder cocaine were Hispanic; more Hispanics than
non-Hispanic White and non-Hispanic Black people received sentences for crimes
related to powder cocaine.

Injection

Drug injection
provides the highest blood levels of drug in the shortest amount of time.
Subjective effects not commonly shared with other methods of administration
include a ringing in the ears moments after injection (usually when in excess of
120 milligrams) lasting 2 to 5
minutes including tinnitus & audio distortion. This is colloquially referred to
as a "bell ringer". In a study of cocaine users, the
average time taken to reach peak subjective effects was 3.1 minutes. The
euphoria passes quickly. Aside from the toxic effects of cocaine, there is also
danger of circulatory emboli from the insoluble substances that may be used to
cut the drug. As with all injected illicit substances, there is a risk of the
user contracting blood-borne infections if sterile injecting equipment is not
available or used.

An injected
mixture of cocaine and heroin, known as “speedball” is a particularly popular
and dangerous combination, as the converse effects of the drugs actually
complement each other, but may also mask the symptoms of an overdose. It has
been responsible for numerous deaths, including celebrities such as John Belushi,
Chris Farley, Mitch Hedberg, River Phoenix and Layne Staley.

Experimentally,
cocaine injections can be delivered to animals such as fruit flies to study the
mechanisms of cocaine addiction.

Smoke

Smoking freebase
or crack cocaine is most often accomplished using a pipe made from a small glass
tube, often taken from "Love roses," small glass tubes with a paper rose that
are promoted as romantic gifts. These are sometimes called "stems", "horns",
"blasters" and "straight shooters". A small piece of clean heavy copper or
occasionally stainless steel scouring pad – often called a "brillo" (actual
Brillo pads contain soap, and are not used), or "chore", named for Chore Boy
brand copper scouring pads, – serves as a reduction base and flow modulator in
which the "rock" can be melted and boiled to vapor. In a pinch, crack smokers
sometimes smoke though a soda can with small holes in the bottom instead of a
crack pipe. Also, the bottoms of small glass liquor bottles can be removed, and
the bottles neck can then be stuffed with chore to use as a makeshift
crack pipe.

Crack is smoked
by placing it at the end of the pipe; a flame held close to it produces vapor,
which is then inhaled by the smoker. The effects, felt almost immediately after
smoking, are very intense and do not last long – usually five to fifteen
minutes. In a study performed on crack cocaine users, the average
time taken for them to reach their peak subjective "high" was 1.4 minutes. Most
(especially frequent) users crave more immediately after the peak. "Crack
houses" depend on these cravings by providing a place for smoking crack to its
users, and a ready supply of small bags for sale.

When smoked,
cocaine is sometimes combined with other drugs, such as cannabis, often rolled
into a joint or blunt.
Powdered cocaine is also sometimes smoked, though heat destroys much of the
chemical; smokers often sprinkle it on marijuana.

The language
referring to paraphernalia and practices of smoking cocaine vary, as do the
packaging methods in the street level sale.

Physical
mechanisms

The difference
between cocaine & amphetamine with regard to DAT1 receptor reuptake blocking.
Cocaine binds directly to the DAT1 transporter, whereas amphetamines
phosphorylate and invert the transporter causing it to internalize.

The
pharmacodynamics of cocaine involve the complex relationships of
neurotransmitters (inhibiting monoamine uptake in rats with ratios of about:
serotonin:dopamine
= 2:3, serotonin:norepinephrine = 2:5) The most extensively studied
effect of cocaine on the central nervous system is the blockade of the dopamine
transporter protein. Dopamine transmitter released during neural signaling is
normally recycled via the transporter; i.e., the transporter binds the
transmitter and pumps it out of the synaptic cleft back into the presynaptic
neuron, where it is taken up into storage vesicles. Cocaine binds tightly at the
dopamine transporter forming a complex that blocks the transporter's function.
The dopamine transporter can no longer perform its reuptake function, and thus
dopamine accumulates in the synaptic cleft. This results in an enhanced and
prolonged postsynaptic effect of dopaminergic signaling at dopamine receptors on
the receiving neuron. Prolonged exposure to cocaine, as occurs with habitual
use, leads to homeostatic dysregulation of normal (i.e. without cocaine)
dopaminergic signaling via down-regulation of dopamine receptors and enhanced
signal transduction. The decreased dopaminergic signaling after chronic cocaine
use may contribute to depressive mood disorders and sensitize this important
brain reward circuit to the reinforcing effects of cocaine (e.g. enhanced
dopaminergic signalling only when cocaine is self-administered). This
sensitization contributes to the intractable nature of addiction and relapse.

Dopamine-rich
brain regions such as the ventral tegmental area, nucleus accumbens, and
prefrontal cortex are frequent targets of cocaine addiction research. Of
particular interest is the pathway consisting of dopaminergic neurons
originating in the ventral tegmental area that terminate in the nucleus
accumbens. This projection may function as a "reward center", in that it seems
to show activation in response to drugs of abuse like cocaine in addition to
natural rewards like food or sex. While the precise role of dopamine
in the subjective experience of reward is highly controversial among
neuroscientists, the release of dopamine in the nucleus accumbens is widely
considered to be at least partially responsible for cocaine's rewarding effects.
This hypothesis is largely based on laboratory data involving rats that are
trained to self-administer cocaine. If dopamine antagonists are infused directly
into the nucleus accumbens, well-trained rats self-administering cocaine will
undergo extinction (i.e. initially increase responding only to stop completely)
thereby indicating that cocaine is no longer reinforcing (i.e. rewarding) the
drug-seeking behavior.

Cocaine's
effects on serotonin (5-hydroxytryptamine, 5-HT) show across multiple serotonin
receptors, and is shown to inhibit the re-uptake of 5-HT3 specifically as an
important contributor to the effects of cocaine. The overabundance of 5-HT3
receptors in cocaine conditioned rats display this trait, however the exact
effect of 5-HT3 in this process is unclear. The 5-HT2 receptor
(particularly the subtypes 5-HT2AR, 5-HT2BR and 5-HT2CR) show influence in the
evocation of hyperactivity displayed in cocaine use.

In addition to
the mechanism shown on the above chart, cocaine has been demonstrated to bind as
to directly stabilize the DAT transporter on the open outward-facing
conformation whereas other stimulants (namely phenethylamines) stabilize the
closed conformation. Further, cocaine binds in such a way as to inhibit a
hydrogen bond innate to DAT that otherwise still forms when amphetamine and
similar molecules are bound. Cocaine's binding properties are such that it
attaches so this hydrogen bond will not form and is blocked from formation due
to the tightly locked orientation of the cocaine molecule. Research studies have
suggested that the affinity for the transporter is not what is involved in
habituation of the substance so much as the conformation and binding properties
to where & how on the transporter the molecule binds.

Sigma receptors
are effected by cocaine, as cocaine functions as a sigma ligand agonist. Further specific receptors it has been demonstrated to function on are
NMDA and the D1 dopamine receptor.

Cocaine also
blocks sodium channels, thereby interfering with the propagation of action
potentials; thus, like lignocaine and novocaine, it acts as a local anesthetic.
Cocaine also causes vasoconstriction, thus reducing bleeding during minor
surgical procedures. The locomotor enhancing properties of cocaine may be
attributable to its enhancement of dopaminergic transmission from the substantia
nigra. Recent research points to an important role of circadian mechanisms and clock genes in behavioral actions of cocaine.

Because nicotine
increases the levels of dopamine in the brain, many cocaine users find that
consumption of tobacco products during cocaine use enhances the euphoria. This,
however, may have undesirable consequences, such as uncontrollable chain smoking
during cocaine use (even users who do not normally smoke cigarettes have been
known to chain smoke when using cocaine), in addition to the detrimental health
effects and the additional strain on the cardiovascular system caused by
tobacco.

In addition to
irritability, mood disturbances, restlessness, paranoia, and auditory
hallucinations, cocaine use can cause several dangerous physical conditions. It
can lead to disturbances in heart rhythm and heart attacks, as well as chest
pains or even respiratory failure. In addition, strokes, seizures and headaches
are common in heavy users.

Cocaine can
often cause reduced food intake, many chronic users lose their appetite and can
experience severe malnutrition and significant weight loss. Cocaine effects,
further, are shown to be potentiated for the user when used in conjunction with
new surroundings and stimuli, and otherwise novel environs.

Metabolism and
excretion

Cocaine is
extensively metabolized, primarily in the liver, with only about 1% excreted
unchanged in the urine. The metabolism is dominated by hydrolytic ester
cleavage, so the eliminated metabolites consist mostly of benzoylecgonine (BE),
the major metabolite, and other significant metabolites in lesser amounts such
as ecgonine methyl ester (EME) and ecgonine. Further minor metabolites of
cocaine include norcocaine, p-hydroxycocaine, m-hydroxycocaine, p-hydroxybenzoylecgonine
(pOHBE), and m-hydroxybenzoylecgonine. These do not include
metabolites created beyond the standard metabolism of the drug in the human
body, like for example by the process of pyrolysis such as is the case with
methylecgonidine.

Depending on
liver and kidney function, cocaine metabolites are detectable in urine.
Benzoylecgonine can be detected in urine within four hours after cocaine intake
and remains detectable in concentrations greater than 150 ng/ml typically for up
to eight days after cocaine is used. Detection of accumulation of cocaine
metabolites in hair is possible in regular users until the sections of hair
grown during use are cut or fall out.

If consumed with
alcohol, cocaine combines with alcohol in the liver to form cocaethylene.
Studies have suggested cocaethylene is both more euphorigenic, and has a higher
cardiovascular toxicity than cocaine by itself.

Cocaine Effects and
Health
Issues

Acute

Cocaine is a
potent central nervous system stimulant. Its effects can last from 20 minutes to
several hours, depending upon the dosage of cocaine taken, purity, and method of
administration.

The initial
signs of stimulation are hyperactivity, restlessness, increased blood pressure,
increased heart rate and euphoria. The euphoria is sometimes followed by
feelings of discomfort and depression and a craving to experience the drug
again. Sexual interest and pleasure can be amplified. Side effects can include
twitching, paranoia,
and impotence, which usually increases with frequent usage.

With excessive
or prolonged use, the drug can cause itching, tachycardia, hallucinations, and
paranoid delusions. Overdoses cause tachyarrhythmias and a marked elevation of
blood pressure. These can be life-threatening, especially if the user has
existing cardiac problems. The LD50 of cocaine when administered to
mice is 95.1 mg/kg. Toxicity results in seizures, followed by
respiratory and circulatory depression of medullar origin. This may lead to
death from respiratory failure, stroke, cerebral hemorrhage, or heart-failure.
Cocaine is also highly pyrogenic, because the stimulation and increased muscular
activity cause greater heat production. Heat loss is inhibited by the intense
vasoconstriction. Cocaine-induced hyperthermia may cause muscle cell destruction
and myoglobinuria resulting in renal failure. Emergency treatment often consists
of administering a benzodiazepine sedation agent, such as diazepam (Valium) to
decrease the elevated heart rate and blood pressure. Physical cooling (ice, cold
blankets, etc...) and paracetamol (acetaminophen) may be used to treat
hyperthermia, while specific treatments are then developed for any further
complications. There is no officially approved specific
antidote for
cocaine overdose, and although some drugs such as dexmedetomidine and rimcazole
have been found to be useful for treating cocaine overdose in animal studies, no
formal human trials have been carried out.

In cases where a
patient is unable or unwilling to seek medical attention, cocaine overdoses
resulting in mild-moderate tachycardia (i.e.: a resting pulse greater than 120
bpm), may be initially treated with 20 mg of orally administered diazepam or
equivalent benzodiazepine (eg: 2 mg lorazepam). Acetaminophen and physical
cooling may likewise be used to reduce mild hyperthermia (<39 C). However, a
history of high blood pressure or cardiac problems puts the patient at high risk
of cardiac arrest or stroke, and requires immediate medical treatment.
Similarly, if benzodiazepine sedation fails to reduce heart rate or body
temperatures fails to lower, professional intervention is necessary.

Cocaine's
primary acute effect on brain chemistry is to raise the amount of dopamine and
serotonin in the nucleus accumbens (the pleasure center in the brain); this
effect ceases, due to metabolism of cocaine to inactive compounds and
particularly due to the depletion of the transmitter resources (tachyphylaxis).
This can be experienced acutely as feelings of depression, as a "crash" after
the initial high. Further mechanisms occur in chronic cocaine use. The "crash"
is accompanied with muscle spasms throughout the body, also known as the
"jitters", muscle weakness, headaches, dizziness, and suicidal thoughts. Not all
users will experience these, but most tend to experience some or all of these
symptoms.

Studies have
shown that cocaine usage during pregnancy triggers premature labor
and may lead to abruptio placentae.

Cocaine can
cause coronary artery spasms which lead to a myocardial infarction. This effect
can happen randomly to any user. The coronary artery spasms can occur on the
user's first usage or any other usage after. The coronary spasms cause the
ectopic ventricular foci of the heart to become hypoxic and the extreme
irritability can trigger life-threatening ventricular arrhythmias.

Chronic

Main effects of
chronic cocaine use.

Chronic cocaine
intake causes brain cells to adapt functionally to strong imbalances of
transmitter levels in order to compensate extremes. Thus, receptors disappear
from the cell surface or reappear on it, resulting more or less in an "off" or
"working mode" respectively, or they change their susceptibility for binding
partners (ligands) – mechanisms called
down-/upregulation.
However, studies suggest cocaine abusers do not show normal age-related loss of
striatal DAT sites, suggesting cocaine has neuroprotective properties for
dopamine neurons. The experience of insatiable hunger, aches,
insomnia/oversleeping, lethargy, and persistent runny nose are often described
as very unpleasant. Depression with suicidal ideation may develop in very heavy
users. Finally, a loss of vesicular monoamine transporters, neurofilament
proteins, and other morphological changes appear to indicate a long term damage
of dopamine neurons. All these effects contribute a rise in tolerance thus
requiring a larger dosage to achieve the same effect.

The lack of
normal amounts of serotonin and dopamine in the brain is the cause of the
dysphoria and depression felt after the initial high. Physical withdrawal is not
dangerous, and is in fact restorative. The diagnostic criteria for cocaine
withdrawal are characterized by a dysphoric mood, fatigue, unpleasant dreams,
insomnia or hypersomnia, erectile dysfunction, increased appetite, psychomotor
retardation or agitation, and anxiety.

Physical side
effects from chronic smoking of cocaine include hemoptysis, bronchospasm,
pruritus, fever, diffuse alveolar infiltrates without effusions, pulmonary and
systemic eosinophilia, chest pain, lung trauma, sore throat, asthma, hoarse
voice, dyspnea (shortness of breath), and an aching, flu-like syndrome. A common
but untrue belief is that the smoking of cocaine chemically breaks down tooth
enamel and causes tooth decay. However, cocaine does often cause involuntary
tooth grinding, known as bruxism, which can deteriorate tooth enamel and lead to
gingivitis.

Chronic
intranasal usage can degrade the cartilage separating the nostrils (the septum
nasi), leading eventually to its complete disappearance. Due to the absorption
of the cocaine from cocaine hydrochloride, the remaining hydrochloride forms a
dilute hydrochloric acid.

Cocaine may also
greatly increase this risk of developing rare autoimmune or connective tissue
diseases such as lupus, Goodpasture's disease, vasculitis, glomerulonephritis,
Stevens-Johnson syndrome and other diseases. It can also cause a
wide array of kidney diseases and renal failure. While these conditions are
normally found in chronic use they can also be caused by short term exposure in
susceptible individuals.

Cocaine abuse
doubles both the risks of hemorrhagic and ischemic strokes, as well
as increases the risk of other infarctions, such as myocardial infarction.

Years after the
abuse has ended, many ex-abusers report a noticeably reduced attention span.

Cocaine as a local
anesthetic

Cocaine was
historically useful as a topical anesthetic in eye and nasal surgery, although
it is now predominantly used for nasal and lacrimal duct surgery. The major
disadvantages of this use are cocaine's intense vasoconstrictor activity and
potential for cardiovascular toxicity. Cocaine has since been largely replaced
in Western medicine by synthetic local anaesthetics such as benzocaine,
proparacaine, lignocaine/xylocaine/lidocaine,
and tetracaine though it remains available for use if specified. If
vasoconstriction is desired for a procedure (as it reduces bleeding), the
anesthetic is combined with a vasoconstrictor such as phenylephrine or
epinephrine. In Australia it is currently prescribed for use as a local
anesthetic for conditions such as mouth and lung ulcers. Some ENT specialists
occasionally use cocaine within the practice when performing procedures such as
nasal cauterization. In this scenario dissolved cocaine is soaked into a ball of
cotton wool, which is placed in the nostril for the 10-15 minutes immediately
prior to the procedure, thus performing the dual role of both numbing the area
to be cauterized and also vasoconstriction. Even when used this way, some of the
used cocaine may be absorbed through oral or nasal mucosa and give systemic
effects.

In 2005,
researchers from Kyoto University Hospital proposed the use of cocaine in
conjunction with phenylephrine administered in the form of an eye drop as a
diagnostic test for Parkinson's disease.

Etymology

The word
"cocaine" was made from "coca" + the suffix "-ine"; from its use as a local
anaesthetic a suffix "-caine" was extracted and used to form names of synthetic
local anaesthetics.

Current
Prohibition

The production,
distribution and sale of cocaine products is restricted (and illegal in most
contexts) in most countries as regulated by the Single Convention on Narcotic
Drugs, and the United Nations Convention Against Illicit Traffic in Narcotic
Drugs and Psychotropic Substances. In the United States the manufacture,
importation, possession, and distribution of cocaine is additionally regulated
by the 1970 Controlled Substances Act.

Some countries,
such as Peru and Bolivia permit the cultivation of coca leaf for traditional
consumption by the local indigenous population, but nevertheless prohibit the
production, sale and consumption of cocaine.

Some parts of
Europe and
Australia allow processed cocaine for medicinal uses only.

Interdiction

In 2004,
according to the United Nations, 589 metric tons of cocaine were seized globally
by law enforcement authorities. Colombia seized 188 tons, the United States
166 tons, Europe 79 tons,
Peru 14 tons,
Bolivia 9 tons, and the rest of the world 133 tons.

Illicit
Cocaine Trade

Bricks of
cocaine, a form in which it is commonly transported.

Because of the
extensive processing it undergoes during preparation, cocaine is generally
treated as a 'hard drug', with severe penalties for possession and trafficking.
Demand remains high, and consequently black market cocaine is quite expensive.
Unprocessed cocaine, such as coca leaves, are occasionally purchased and sold,
but this is exceedingly rare as it is much easier and more profitable to conceal
and smuggle it in powdered form. The scale of the market is immense: 770 tonnes
times $100 per gram retail = up to $77 billion.

Production

Colombia is the
world's leading producer of cocaine. Due to Colombia's 1994
legalization of small amounts of cocaine for personal use, while sale of cocaine
was still prohibited, the result was the spread of local coca crops, partly
justified by the local demand.

Three-quarters
of the world's annual yield of cocaine has been produced in Colombia, both from
cocaine base imported from Peru (primarily the Huallaga Valley) and Bolivia, and
from locally grown coca. There was a 28% increase from the amount of potentially
harvestable coca plants which were grown in Colombia in 1998 . This, combined
with crop reductions in Bolivia and Peru, made Colombia the nation with the
largest area of coca under cultivation after the mid-1990s. Coca grown for
traditional purposes by indigenous communities, a use which is still present and
is permitted by Colombian laws, only makes up a small fragment of total coca
production, most of which is used for the illegal drug trade.

Attempts to
eradicate coca fields through the use of defoliants have devastated part of the
farming economy in some coca growing regions of Colombia, and strains appear to
have been developed that are more resistant or immune to their use. Whether
these strains are natural mutations or the product of human tampering is
unclear. These strains have also shown to be more potent than those previously
grown, increasing profits for the drug cartels responsible for the exporting of
cocaine. Although production fell temporarily, coca crops rebounded as numerous
smaller fields in Colombia, rather than the larger plantations.

The cultivation
of coca has become an attractive, and in some cases even necessary, economic
decision on the part of many growers due to the combination of several factors,
including the persistence of worldwide demand, the lack of other employment
alternatives, the lower profitability of alternative crops in official crop
substitution programs, the eradication-related damages to non-drug farms, and
the spread of new strains of the coca plant.

Synthesis

Synthetic
cocaine would be highly desirable to the illegal drug industry, as it would
eliminate the high visibility and low reliability of offshore sources and
international smuggling, replacing them with clandestine domestic laboratories,
as are common for illicit
methamphetamine. However, natural cocaine remains the lowest cost and
highest quality supply of cocaine.

Note, names like
'synthetic cocaine' and 'new cocaine' have been misapplied to phencyclidine
(PCP) and various designer drugs.

Trafficking and
distribution

Cocaine smuggled
in a charango, 2008.

Organized
criminal gangs operating on a large scale dominate the cocaine trade. Most
cocaine is grown and processed in South America, particularly in Colombia,
Bolivia, Peru, and smuggled into the United States and Europe, the United States
being the worlds largest consumer of Cocaine, where it is sold at
huge markups; usually in the US at $50-$75 for 1 gram (or a "fitty rock"), and
$125-200 for 3.5 grams (1/8th of an ounce, or an "eight ball").

Cocaine
shipments from South America transported through Mexico or Central America are
generally moved over land or by air to staging sites in northern Mexico. The
cocaine is then broken down into smaller loads for smuggling across the
U.S.–Mexico border.
The primary cocaine importation points in the United States are in Arizona,
southern California, southern Florida, and Texas. Typically, land vehicles are
driven across the U.S.-Mexico border. Sixty Five percent of cocaine enters the
United States through Mexico, and the vast majority of the rest enters through
Florida.

Cocaine is also
carried in small, concealed, kilogram quantities across the border by couriers
known as “mules” (or “mulas”), who cross a border either legally, e.g. through a
port or airport, or illegally through undesignated points along the border. The
drugs may be strapped to the waist or legs or hidden in bags, or hidden in the
body. If the mule gets through without being caught, the gangs will reap most of
the profits. If he or she is caught however, gangs will sever all links and the
mule will usually stand trial for trafficking by him/herself.

Cocaine
traffickers from Colombia, and recently Mexico, have also established a
labyrinth of smuggling routes throughout the Caribbean, the Bahama Island chain,
and South Florida. They often hire traffickers from Mexico or the Dominican
Republic to transport the drug. The traffickers use a variety of smuggling
techniques to transfer their drug to U.S. markets. These include airdrops of
500–700 kg in the Bahama Islands or off the coast of Puerto Rico, mid-ocean
boat-to-boat transfers of 500–2,000 kg, and the commercial shipment of tonnes of
cocaine through the port of Miami.

Bulk cargo ships
are also used to smuggle cocaine to staging sites in the western Caribbean–Gulf
of Mexico area. These vessels are typically 150–250-foot (50–80 m) coastal
freighters that carry an average cocaine load of approximately 2.5 tonnes.
Commercial fishing vessels are also used for smuggling operations. In areas with
a high volume of recreational traffic, smugglers use the same types of vessels,
such as go-fast boats, as those used by the local populations.

Sophisticated
drug subs are the latest tool drug runners are using to bring cocaine north from
Colombia, it was reported on March 20, 2008. Although the vessels were once
viewed as a quirky sideshow in the drug war, they are becoming faster, more
seaworthy, and capable of carrying bigger loads of drugs than earlier models,
according to those charged with catching them.

Sales to consumers

Cocaine is
readily available in all major countries' metropolitan areas. According to the
Summer 1998 Pulse Check, published by the U.S. Office of National Drug
Control Policy, cocaine use had stabilized across the country, with a few
increases reported in San Diego, Bridgeport, Miami, and Boston. In the West,
cocaine usage was lower, which was thought to be due to a switch to
methamphetamine among some users; methamphetamine is cheaper and provides a
longer-lasting high. Numbers of cocaine users are still very large, with a
concentration among urban youth.

In addition to
the amounts previously mentioned, cocaine can be sold in "bill sizes": for
example, $10 might purchase a "dime bag," a very small amount (0.1–0.15 g) of
cocaine. Twenty dollars might purchase .15–.3 g. However, in lower Texas, it's
sold cheaper due to it being easier to receive: a dime for $10 is .4g, a 20 is
.8-1.0 gram and a 8-ball (3.5g) is sold for $60 to $80 dollars, depending on the
quality and dealer. These amounts and prices are very popular among young people
because they are inexpensive and easily concealed on one's body. Quality and
price can vary dramatically depending on supply and demand, and on geographic
region.

However, UK
prices are astronomical compared to those in the USA, with £40 (typically $80)
getting 1 gram of cocaine (compared to $20-$40 in the USA).

The European
Monitoring Centre for Drugs and Drug Addiction reports that the typical retail
price of cocaine varied between 50€ and 75€ per gram in most European countries,
although Cyprus, Romania, Sweden and Turkey reported much higher values.

Bags of cocaine,
adulterated with fruit flavoring.

Consumption

World annual
cocaine consumption currently stands at around 600 metric tons, with the United
States consuming around 300 metric tons, 50% of the total, Europe about 150
metric tons, 25% of the total, and the rest of the world the remaining 150
metric tons or 25%.

Cocaine
Adulterants

Cocaine is "cut"
with many substances such as:

Anesthetics:

Lidocaine

Benzocaine

Procaine

Other
stimulants:

Caffeine

Ephedrine

Methamphetamine

Inert powder:

Baking soda

Inositol

Cocaine Usage

According to a
2007 United Nations report, Spain is the country with the highest rate of
cocaine usage (3.0% of adults in the previous year). Other countries
where the usage rate meets or exceeds 1.5% are the United States (2.8%), England
and Wales (2.4%), Canada (2.3%), Italy (2.1%), Bolivia (1.9%), Chile (1.8%), and
Scotland (1.5%).

In the United
States

General usage

Cocaine is the
second most popular illegal recreational drug in the U.S. (behind marijuana) and the U.S. is the world's largest consumer of cocaine.
Cocaine is commonly used in middle to upper class communities. It is also
popular amongst college students, to aid in studying and as a party drug. Its
users span over different ages, races, and professions. In the 1970s and 80's,
the drug became particularly popular in the disco culture as cocaine usage was
very common and popular in many discos such as Studio 54.

The National
Household Survey on Drug Abuse (NHSDA) reported in 1999 that cocaine was used by
3.7 million Americans, or 1.7% of the household population age 12 and older.
Estimates of the current number of those who use cocaine regularly (at least
once per month) vary, but 1.5 million is a widely accepted figure within the
research community.

Although cocaine
use had not significantly changed over the six years prior to 1999, the number
of first-time users went up from 574,000 in 1991, to 934,000 in 1998 – an
increase of 63%. While these numbers indicated that cocaine is still widely
present in the United States, cocaine use was significantly less prevalent than
it was during the early 1980s.

Usage among
youth

The 1999
Monitoring the Future (MTF) survey found the proportion of American students
reporting use of powdered cocaine rose during the 1990s. In 1991, 2.3% of
eighth-graders stated that they had used cocaine in their lifetime. This figure
rose to 4.7% in 1999. For the older grades, increases began in 1992 and
continued through the beginning of 1999. Between those years, lifetime use of
cocaine went from 3.3% to 7.7% for tenth-graders and from 6.1% to 9.8% for high
school seniors. Lifetime use of crack cocaine, according to MTF, also increased
among eighth-, tenth-, and twelfth-graders, from an average of 2% in 1991 to
3.9% in 1999.

Perceived risk
and disapproval of cocaine and crack use both decreased during the 1990s at all
three grade levels. The 1999 NHSDA found the highest rate of monthly cocaine use
was for those aged 18–25 at 1.7%, an increase from 1.2% in 1997. Rates declined
between 1996 and 1998 for ages 26–34, while rates slightly increased for the
12–17 and 35+ age groups. Studies also show people are experimenting with
cocaine at younger ages. NHSDA found a steady decline in the mean age of first
use from 23.6 years in 1992 to 20.6 years in 1998.